Paraoxonase activity and dementia

Wehr, H; Bednarska-Makaruk, Małgorzata; Graban, Ałła; Lipczyńska-Łojkowska, Wanda; Rodo, M; Bochyńska, Anna; Ryglewicz, Danuta

doi:10.1016/j.jns.2009.02.317

Cited by 56 publications

(44 citation statements)

References 10 publications

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“…These results point to a significant role of oxidative stress in the forms of dementia with prevalent neurodegeneration. 96 Similar findings were obtained in a study that included patients with either AD or vascular dementia. 97 PON1…”

Section: 70-73supporting

confidence: 75%

Paraoxonase 1 in neurological disorders

Menini

Gugliucci

2013

Redox Report

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Paroxonase 1 displays multiple physiological activities that position it as a putative player in the pathogenesis of neurological disorders. Here we reviewed the literature focusing on the role of paraoxonase 1 (PON1) as a factor in the risk of stroke and the major neurodegenerative diseases. PON1 activity is reduced in stroke patients, which significantly correlates inversely with carotid and cerebral atherosclerosis. The presence of the R allele of the Q192R PON1 polymorphism seems to potentiate this risk for stroke. PON1 exerts peroxidase activities that may be important in neurodegenerative disorders associated with oxidative stress. PON1 is also a key detoxifier of organophosphates and organophosphate exposure has been linked to the development of neurological disorders in which acetylcholine plays a significant role. In Parkinson's disease most of the studies suggest no participation of either L55M or the Q192R polymorphisms in its pathogenesis. However, many studies suggest that the MM55 PON1 genotype is associated with a higher risk for Parkinson's disease in individuals exposed to organophosphates. In Alzheimer's disease most studies have failed to find any association between PON1 polymorphisms and the development of the disease. Some studies show that PON1 activity is decreased in patients with Alzheimer's disease or other dementias, suggesting a possible protective role of PON1. No links between PON1 polymorphisms or activity have been found in other neurodegenerative diseases such as multiple sclerosis and amyotrophic lateral sclerosis. PON1 is a potential player in the pathogenesis of several neurological disorders. More research is warranted to ascertain the precise pathogenic links and the prognostic value of its measurement in neurological patients.

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Section: 70-73supporting

confidence: 75%

Paraoxonase 1 in neurological disorders

Menini

Gugliucci

2013

Redox Report

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“…It possesses organophosphatase, arylesterase and lactonase activities [60] and exerts peroxidase activities that may be important in neurodegenerative disorders associated with oxidative stress [26]. Plasma levels of this enzyme decreases in neurological diseases such as multiple sclerosis during relapse [61], major depression [62], patients with Alzheimer's disease or other dementias [63] [64]. In the present study, we observed significantly decreased arylesterase activity in serum of autistic children.…”

Section: Discussionsupporting

confidence: 57%

Nuclear Factor-Kappa B and Other Oxidative Stress Biomarkers in Serum of Autistic Children

Abdel-Salam¹,

Youness²,

Mohammed³

et al. 2015

OJMIP

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The aim of the present study was to investigate the status of oxidative stress in the serum of children affected with autism spectrum disorder. Twenty autistic children aged 3 to 12 years, were gender and age-matched with 20 typically developing children. Changes in the levels of the redox-sensing transcription factor nuclear factor-kappa B (NF-κB) was measured in serum of autistic children and controls. Other oxidative stress biomarkers such as malondialdehyde, reduced glutathione, total antioxidant capacity, catalase activity, and paraoxonase 1 activity were determined in serum as well. Significant increase was observed in serum NF-κB of autistic children compared to that in controls (by 138.6%). There was also marked increase in malondialdehyde level by 87.3% in autistic patients. Meanwhile, there were significant decreases in reduced glutathione (by 24%), catalase activity (by 40.8%), paraoxonase 1 activity (by 36.6%), and total antioxidant capacity (by 36.5%) compared to the control group. These data clearly demonstrate increased oxidative stress in serum of autistic children and suggest that the NF-κB signaling pathway is activated in autism, possibly due to increased oxidative burden.

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“…Several PON1 polymorphisms have been shown to influence the risk for developing PD; carriers of slow metabolizer and lower-activity variants leading to decreased PON1 expression levels are likely to be most susceptible to pesticide exposures. [71][72][73][74] Decreased serum enzyme activity was also found in a number of neurodegenerative conditions, such as dementia 75,76 or multiple sclerosis. 77 Here, we demonstrate that the administration of cerebrolysin was able to reverse the marked decline in the activity of the enzyme induced by rotenone in several brain regions.…”

mentioning

confidence: 99%

Cerebrolysin protects against rotenone-induced oxidative stress and neurodegeneration

Abdel-Salam¹,

Mohammed²,

Youness³

et al. 2014

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Abstract:We investigated the effect of cerebrolysin, a peptide mixture used for promoting memory and recovery from cerebral stroke, on the development of oxidative stress and nigrostriatal cell injury induced by rotenone administration in rats. Rotenone 1.5 mg/kg was given subcutaneously three times weekly either alone or in combination with cerebrolysin at 21.5, 43, or 86 mg/kg. Rats were euthanized 14 days after starting the rotenone injection. Lipid peroxidation (malondialdehyde), reduced glutathione (GSH), nitric oxide (nitrite) concentrations, paraoxonase 1 (PON1), and acetylcholinesterase (AChE) activities -as well as the monocyte chemoattractant protein-1 (MCP-1) and the antiapoptotic protein Bcl-2 -were measured in the brain. Histopathology, tyrosine hydroxylase, inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and cleaved caspase-3 immunohistochemistry were also performed. Rotenone caused a significantly elevated oxidative stress and proinflammatory response in the different brain regions. Malondialdehyde and nitric oxide concentrations were significantly increased, while GSH markedly decreased in the cerebral cortex, striatum, hippocampus, and in the rest of the brain. PON1 and AChE activities significantly decreased with respect to the control levels after rotenone application. Striatal Bcl-2 was significantly decreased while MCP-1 increased following rotenone injection. Rotenone caused prominent iNOS, TNF-α, and caspase-3 immunostaining in the striatum and resulted in markedly decreased tyrosine hydroxylase immunoreactivity in the substantia nigra and striatum. Cerebrolysin coadministered with rotenone decreased lipid peroxidation, increased GSH, and inhibited the elevation of nitric oxide induced by rotenone. Cerebrolysin also decreased the rotenone-induced decline in the PON1 and AChE activities and the rotenone-mediated changes in the striatal Bcl-2 and MCP-1 levels. The drug reduced iNOs, TNF-α, and caspase 3 expressions and increased the tyrosine hydroxylase immunoreactivity in the striatum. Cerebrolysin markedly prevented the development of neuronal damage in the cortex and striatum. These data suggest that cerebrolysin may have potential therapeutic effect in Parkinson's disease.

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Paraoxonase activity and dementia

Cited by 56 publications

References 10 publications

Paraoxonase 1 in neurological disorders

Paraoxonase 1 in neurological disorders

Nuclear Factor-Kappa B and Other Oxidative Stress Biomarkers in Serum of Autistic Children

Cerebrolysin protects against rotenone-induced oxidative stress and neurodegeneration

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